Pat Salber blogging from the American Diabetes Association annual meeting.

I am at the 2006 American Diabetes Association annual Scientific Sessions for the next 4 days, so I will be blogging on great new stuff being discussed at this meeting—the premier scientific meeting in the field of diabetes.

I attended a very interesting symposium on “ectopic” fat and its relationship to insulin resistance and type 2 diabetes. The term “ectopic” fat means there is fat deposited in parts of the body where it doesn’t belong. It is believed to be one of causes of the metabolic problems that occur in people with or at risk for Type 2 diabetes.

The first presentation at this symposium described how fat deposits in the liver lead to insulin resistance. We have known for years that “central obesity” is a risk factor for Type 2 diabetes. Remember the warnings that fat in an “apple” pattern is worse for us than fat in a “pear” pattern?. But it isn’t that subcutaneous fat (fat deposited below the skin) that’s really bad for us, rather it is fat inside the abdominal cavity, called visceral fat, that increases our risk for heart disease, stroke and type 2 diabetes. Now we know that the worst fat may be the fat that gets deposited in our organs—fat in our liver cells, fat in our muscle cells, and maybe, fat deposited in our heart cells.

Another presentator on this first day of the ADA meetings talked about the toxic effect of excess fat on the beta cells. The beta cells are the cells that produce insulin, the major regulator of blood sugar and other important aspects of our metabolism. It turns out that fat is toxic to beta cells when there is also high blood sugar (blood glucose) levels. This condition is known as "glucolipotoxicity" (translation: toxicity because of combined high glucose and high fat concentrations in the blood). This one of the reasons why people with type 2 diabetes, who initially produce very high levels of insulin to compensate for their insulin resistance ultimately lose their ability to secrete enough insulin to keep blood sugars normal. It occurs because of beta cells are poisoned and die (called "apoptosis" - pronounced "a pop toe sis") because of the high glucose and lipid levels. Some clinicians refer to this process as "burning out the beta cells." Loss of beta cells can lead to someone with type 2 diabetes having to take insulin shots, instead of blood glucose lowering pills, to control their blood sugars.. The information in this presentation provides a compelling reason for everyone with type 2 diabetes to do their best to keep their glucose and lipid levels in good control with diet, exercise, glucose-lowering, and lipid-lowering medications. Here's the mantra: "Beta cells are our friends. Let's save them as long as we can!"

The last presentation of this symposium discussed the effects of exercise on deposits of fat in muscle cells. Obesity and type 2 diabetes is associated with deposits of large globules of fat in muscles. Fat in muscles leads to those cells becoming resistant to insulin. Exercise decreases the size of fat globules in muscle cells and is associated with improved muscle cell sensitivity to insulin.

Insulin resistant people who have fat deposits in the cells of key organs improve their sensitivity to insulin when they diet, lose weight, and decrease the fat inside of their cells. So new news. Fat in the wrong places is bad for us. Not so new news, weight loss and exercise can reverse many of the adverse effects related to central obesity.